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SP1‐induced lncRNA FOXD3‐AS1 contributes to tumorigenesis of cervical cancer by modulating the miR‐296‐5p/HMGA1 pathway
Author(s) -
Ma Wenguang,
Shi Simao,
Chen Lu,
Lou Ge,
Feng Xiaoling
Publication year - 2021
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.29846
Subject(s) - gene knockdown , long non coding rna , downregulation and upregulation , cancer research , competing endogenous rna , carcinogenesis , biology , metastasis , cell growth , tumor progression , glioma , cancer , apoptosis , gene , genetics
Long noncoding RNAs (lncRNAs) have drawn growing attention due to their regulatory roles in various diseases, including tumors. Recently, lncRNA FOXD3 antisense RNA 1 (FOXD3‐AS1) was shown to be overexpressed in colon adenocarcinoma and glioma, exerting oncogenic functions. However, its expression and effects in cervical cancer (CC) remained unknown. In this research, our group first reported that the levels of FOXD3‐AS1 were distinctly elevated in CC samples and cell lines. The distinct upregulation of FOXD3‐AS1 was associated with lymphatic invasion, distant metastasis, and International Federation of Gynecology and Obstetrics stage, and also predicted poor clinical results of CC patients. Next, transcription factor SP1 was demonstrated to resulting in the upregulation of FOXD3‐AS1 in CC. Functional assays indicated that knockdown of FOXD3‐AS1 distinctly suppressed CC progression via affecting cell proliferation, cell apoptosis, and metastasis. Moreover, mechanistic studies suggested that FOXD3‐AS1 acted as an endogenous sponge by directly binding miR‐296‐5p, resulting in the suppression of miR‐296‐5p. In addition, we also reported that high mobility group A, a direct target of miR‐296‐5p, could mediate the tumor‐promotive effects that FOXD3‐AS1 displayed. Overall, our present study might help to lead a better understanding of the pathogenesis of CC, provide a novel possible tumor biomarker, and probe the feasibility of lncRNA‐directed treatments for CC.